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The Intracellular Site of Action of Insulin: The Mitochondrial Krebs Cycle

1989; Academic Press; Linguagem: Inglês

10.1016/b978-0-12-152830-0.50006-2

0070-2137

Chandra Mohan, Paul J. Geiger, Samuel P. Bessman,

Diet and metabolism studies

This chapter discusses the intracellular site of action of insulin involving the mitochondrial Krebs cycle. To begin with, there is at present no coherent model that accounts, through the process of partial phosphorylation or dephosphorylation of enzymes or other proteins, for all of the manifold actions of insulin on cells. It is known that insulin stimulates the uptake of glucose most effectively in fat cells in which mitochondria are close to the plasma membrane. Also, much evidence has accumulated to show that insulin reverses the net catabolism of protein, glycogen, and fat and promotes their build up and storage. Furthermore, insulin stimulates the incorporation into protein of primarily those pyruvate carbons that are converted to glutamic acid through the Krebs cycle. Insulin has a far greater stimulatory effect on the incorporation into protein of the methylene carbons of succinate than the carboxyl carbons. This can be attributed to the fact that carbons 2 and 3 of succinate either reenter the cycle as acetyl-CoA or remain in the mitochondrial Krebs cycle for a second or third opportunity to be converted to glutamate by the transamination of α-KG.